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MacLeod, M. K. L.

Publications and source records attributed to MacLeod, M. K. L..

3 recordsLinked to original sources

Ovothiol is a redundant part of a complex thiol network in promastigote Leishmania mexicana

A gene encoding OvoA, a key enzyme involved in the biosynthesis of ovothiol, was excised form the genome of Leishmania mexicana promastigotes using CRISPR/cas mediated gene editing. The role of the enzyme in synthesising ovothiol was confirmed since both ovothiol A and ovothiol B were lost from the metabolome of the modified cells. The OvoA knockout line had similar growth kinetics to wild-type progenitor cells and, moreover, most of the changes in metabolism that accompanied the transition of log stage growth to stationary phase were mirrored in the KO line. Significant differences, however, were observed in the ratio of the reduced and oxidised forms of the other major low molecular weight thiols, glutathione and trypanothione, indicative of a role of these other thiols in maintaining reduced ovothiol and demonstrating an interconnected network of low molecular weight thiols in these cells. The OvoA knockout cells remained infective to macrophages where promastigotes transformed to amastigote forms in a manner similar to wild-type. The knockout line was tested for sensitivity to a range of current anti-leishmanial drugs and oxidative and nitrosative stresses. While generally the absence of ovothiol caused little or no change in sensitivity to these stress-inducing agents, enhanced sensitivity to amphotericin B was noted. Author summaryOvothiol is a low molecular weight histidine-derived thiol first described in sea urchin eggs, and later found in many organisms, including the protozoa of the order Kinetoplastida, that includes human pathogens such as the Leishmania species that cause leishmaniasis. Thiol metabolism in the Kinetoplastidae has been studied in some detail, particularly with regard to an unusual bis-glutathione, spermidine conjugate named trypanothione that takes on many of the roles performed by glutathione in most other organisms. Roles for ovothiol in Leishmania have not been previously defined, although potential roles in defence against oxidative stress have been hypothesised. A gene encoding the first enzyme of the pathway involved in ovothiol production, OvoA, was excised from the Leishmania mexicana genome. Its role in ovothiol synthesis was confirmed as ovothiol was absent from the mutants. Little changed, however, with respect to the phenotype of these cells, including their proliferation rate, their ability to infect macrophages or their sensitivity to a range of stress inducing agents. These included several leishmanicidal drugs, oxidative and nitrosative stresses. For amphotericin B, however, the Ovothiol lacking cells were more sensitive than wild-type indicating some role in defence against the impact of this drug.

biochemistry↗

Zoonotic avian influenza viruses evade human BTN3A3 restriction

Cross-species transmission of avian influenza A viruses (IAVs) into humans could represent the first step of a future pandemic1. Multiple factors limiting the spillover and adaptation of avian IAVs in humans have been identified, but they are not sufficient to explain which virus lineages are more likely to cross the species barrier1,2. Here, we identified human BTN3A33 (butyrophilin subfamily 3 member A3) as a potent inhibitor of avian but not human IAVs. We determined that BTN3A3 is constitutively expressed in human airways and its antiviral activity evolved in primates. We show that BTN3A3 restriction acts at the early stages of virus replication by inhibiting avian IAV vRNA transcription. We identified residue 313 in the viral nucleoprotein (NP) as the genetic determinant of BTN3A3 sensitivity (313F, or rarely 313L in avian viruses) or evasion (313Y or 313V in human viruses). However, several serotypes of avian IAVs that spilled over into humans in recent decades evade BTN3A3 restriction. In these cases, BTN3A3 evasion is due to substitutions (N, H or Q) in NP residue 52 that is adjacent to residue 313 in the NP structure4. Importantly, we identified more than 150 avian IAV lineages with a BTN3A3-resistant genotype. In conclusion, sensitivity or resistance to BTN3A3 is another factor to consider in the risk assessment of the zoonotic potential of avian influenza viruses.

microbiology↗

Regulatory T cells control the dynamic and site-specific T helper bias following Salmonella infection

FoxP3+ regulatory T cells (Tregs) control inflammation and maintain mucosal homeostasis, but their functions during infection are poorly understood. Th1, Th2 and Th17 cells can be identified by master transcription factors (TFs) T-bet, GATA3 and ROR{gamma}T; Tregs also express these TFs. While T-bet+ Tregs can selectively suppress Th1 cells, it is unclear whether distinct Treg populations can alter Th bias. To address this, we used Salmonella enterica serotype Typhimurium to induce non-lethal colitis. Following infection, we observed an early colonic Th17 response within total CD4 T cells, followed by a Th1 bias. The early Th17 response, which contains both Salmonella-specific and non-Salmonella-specific cells, parallels an increase in T-bet+ Tregs. Later, Th1 cells and ROR{gamma}T+ Tregs dominate. This reciprocal dynamic may indicate that Tregs selectively suppress Th cells, shaping the immune response. Treg depletion 1-2 days post-infection shifted the early Th17 response to a Th1 bias; however, depletion 6-7 days post-infection abrogated the Th1 bias. Thus, Tregs are necessary for the early Th17 response, and for a maximal Th1 response later. These data show that Tregs shape the overall tissue CD4 T cell response and highlight the potential for subpopulations of Tregs to be used in targeted therapeutic approaches.

immunology↗